PE Flashcards
Primary mechanism by which PE causes a CA
Clot in pulmonary artery leads to increased RV afterload (leading to pulmonary HTN and RV failure) as well as reduced venous return to left heart. This causes the IV septum to push to the left. Decreased diastolic filling of the left heart so reduced end diastolic volume. Ultimately get obstructive cardiogenic shock
In terms of the respiratory system, how does a PE lead to a respiratory alkalosis
Clot in pulmonary artery = decreased distal blood flow to areas of lung = ventilated but not perfused (deadspace) = hypoxia = hyperventilate = respiratory alkalosis
Describe the path of a clot from DVT to PE
DVT to IVC to RA to RV to pulmonary trunk to pulmonary artery
What are the signs of a PE on ECG
Prominent S (lead 1), Q wave (lead 3), inverted T (lead 3)
Sinus tachycardia
RBBB
T wave inversion (V1/V2 worst as give best view of RV)
What are some differentials for S1Q3T3 pattern on ECG
PE, bronchospasm, pneumothorax, ARDS
Capnograpgy results in a PE are?
Low ETCO2 (deadspace means reduced ability to eliminate CO2)
What would an echo of a PE show?
Enlarged RV, underfilled and D shaped LV, tricuspid regurg, IV septum either flattened or bulging with paradoxical movement
How would you manage a CA due to PE
Fibrinolytic eg Alteplase
Continue CPR for 60-90 minutes
ECMO, surgical embolectomy or mechanical thrombectomy
How do fibrinolytic work?
Plasminogen activator converting plasminogen to plasmin which converts the fibrin clot to its degradation products
What rhythm do patients in arrest from a PE most commonly present with
PEA